title: Nuclear factor-κB/Bcl-XL pathway is involved in the protective effect of hydrogen-rich saline on the brain following experimental subarachnoid hemorrhage in rabbits.
abstract: Early brain injury (EBI), a significant contributor to poor outcome after subarachnoid hemorrhage (SAH), is intimately associated with neuronal apoptosis. Recently, the protective role of hydrogen (H2 ) in the brain has been widely studied, but the underlying mechanism remains elusive. Numerous studies have shown nuclear factor-κB (NF-κB) as a crucial survival pathway in neurons. Here we investigated the role of H2 in EBI following SAH, focusing on the NF-κB pathway. A double blood injection model was used to produce experimental SAH, and H2 -rich saline was injected intraperitoneally. NF-κB activity within the occipital cortex was measured. Immunofluorescence was performed to demonstrate the activation of NF-κB; Bcl-xL and cleaved caspase-3 were determined via Western blot. Gene expression of Bcl-xL was detected by real-time PCR, and TUNEL and Nissl staining were performed to illustrate brain injury in the occipital cortex. SAH induced a significant increase of cleaved caspase-3. Correspondingly, TUNEL staining demonstrated obvious neuronal apoptosis following SAH. In contrast, H2 treatment markedly increased NF-κB activity and the expression of Bcl-xL and decreased the level of cleaved caspase-3. Additionally, H2 treatment significantly reduced post-SAH neuronal apoptosis. The current study shows that H2 treatment alleviates EBI in the rabbits following SAH and that NF-κB/Bcl-xL pathway is involved in the protective role of H2 .
authors.affiliation: Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, Jiangsu, People's Republic of China.
authors.forename: Zong
authors.initials: Z
authors.lastname: Zhuang
authors.forename: Xue-jun
authors.initials: XJ
authors.lastname: Sun
authors.forename: Xing
authors.initials: X
authors.lastname: Zhang
authors.forename: Huan-dong
authors.initials: HD
authors.lastname: Liu
authors.forename: Wan-chun
authors.initials: WC
authors.lastname: You
authors.forename: Chi-yuan
authors.initials: CY
authors.lastname: Ma
authors.forename: Lin
authors.initials: L
authors.lastname: Zhu
authors.forename: Meng-liang
authors.initials: ML
authors.lastname: Zhou
authors.forename: Ji-xin
authors.initials: JX
authors.lastname: Shi
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D004195:Disease Models, Animal; D024202:Electrophoretic Mobility Shift Assay; D006859:Hydrogen / Q000494:pharmacology*; D020287:In Situ Nick-End Labeling; D008297:Male; D016328:NF-kappa B / Q000378:metabolism*; D018696:Neuroprotective Agents / Q000494:pharmacology*; D011817:Rabbits; D060888:Real-Time Polymerase Chain Reaction; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*; D012965:Sodium Chloride / Q000737:chemistry / Q000494:pharmacology; D013345:Subarachnoid Hemorrhage / Q000378:metabolism*; D051020:bcl-X Protein / Q000378:metabolism*
chemical_list: D016328:NF-kappa B; D018696:Neuroprotective Agents; D051020:bcl-X Protein; D012965:Sodium Chloride; D006859:Hydrogen
keywords: NF-κB/Bcl-xL; apoptosis; early brain injury; hydrogen; subarachnoid hemorrhage